From Wellens’ syndrome to acute anterior myocardial infarction,what is required? Only time!

Abstract

The hallmark of Wellens' syndrome is a distinct modification in the precordial T wave of the electrocardiogram (ECG), which usually indicates substantial stenosis of the proximal left anterior descending artery (LAD). Patients with Wellens' syndrome commonly do not exhibit any symptoms of chest pain. This current case report describes a male patient in his early 60s who presented with sporadic chest pain who was subsequently diagnosed with Wellens’ syndrome-related electrocardiographic abnormalities. In the precordial leads V2–V5, an inverted symmetric T wave was visible on the asymptomatic ECG. The inverted symmetric T wave of the precordial lead V2–V5 reverted back to being upright when the chest pain started. A follow-up ECG performed before emergency surgery revealed ventricular premature beats and an increase of 0.1–0.5 mV in the ST segment of the precordial leads V1–V5. A drug-eluting stent was inserted after the patient's coronary angiography revealed proximal stenosis of the LAD. To prevent acute myocardial infarction, emergency physicians must identify the ECG signs of Wellens’ syndrome and treat high-risk patients with revascularization as soon as feasible. Early recognition and proactive intervention are crucial, as they may help to alleviate adverse consequences.

Introduction

An abnormal electrocardiographic (ECG) pattern known as Wellens’ syndrome is linked to significant proximal left anterior descending artery (LAD) stenosis. Patients with Wellens’ syndrome require early revascularization because, in the majority of cases, LAD stenosis occurs within a few hours after admission in untreated patients.^1–3 This current case report describes a patient in whom Wellens’ syndrome was detected on their ECG, but it was not promptly recognized and revascularized. The patient experienced an acute anterior wall myocardial infarction that was successfully treated using a percutaneous coronary intervention.

Case report

In January 2024, a male patient in his early 60s presented to the Emergency Department, Tianjin First Central Hospital, Tianjin, China with intermittent compression chest pain for 3 days, as well as radiating pain in his shoulders and back. He had a history of hypertension, stroke and receiving peritoneal dialysis for end-stage renal disease. His vital signs were stable upon arrival in the emergency room as follows: blood pressure 135/98 mmHg; heart rate 65 beats per min; 100% oxygen saturation level. When the patient first came to the emergency room, he was not in any pain. The patient had chest pain once more after the first ECG revealed a deep inverted symmetric T wave in the precordial leads V2–V5 (Figure 1(a)). The ECG demonstrated that the inverted symmetric T wave of the precordial lead V2–V5 reverted back to being upright, accompanied by ventricular premature beats (Figure 1(b)). The diagnosis of type B Wellens’ syndrome was tentatively made. Patients typically require an invasive evaluation due to their increased risk of anterior myocardial infarction and severe left anterior descending artery stenosis. The ECG revealed precordial leads V1–V5 ST segment elevation of 0.1–0.5 mV, accompanied by ventricular premature beats, which suggested acute anterior ST segment elevation myocardial infarction (Figure 1(c)). This was reviewed while waiting for emergency surgery in the emergency room and during blood sampling. Severe coronary artery disease affecting the proximal LAD was discovered during his coronary angiography (Figure 2(a)). A drug-eluting stent was inserted and he recovered well (Figure 2(b)). On the ECG on the following day (Figure 1(d)), there was evidence of an anterior myocardial infarction. Following percutaneous coronary intervention, the patient's echocardiogram revealed a 38% ejection fraction and the disappearance of the left ventricular anterior wall and the interventricular septum's motion amplitude. Throughout their hospital stay, the patient did not experience any chest pain. Eventually, the patient's clinical status improved and he was allowed to leave the hospital. When the patient was re-evaluated approximately 1 month later, he showed no signs of angina pectoris or chest pain.

Figure 1.

Electrocardiograms (ECG) of a male patient in his early 60s who presented with intermittent compression chest pain for 3 days, as well as radiating pain in his shoulders and back: (a) ECG when the patient first arrived in the emergency room revealed a deep inverted symmetric T wave in the precordial leads V2–V5; (b) ECG during chest pain attacks revealed that the inverted symmetric T wave of the precordial lead V2–V5 reverted back to being upright, accompanied by ventricular premature beats; (c) ECG prior to stenting revealed precordial leads V1–V5 ST segment elevation of 0.1–0.5 mV, accompanied by ventricular premature beats, which suggested acute anterior ST segment elevation myocardial infarction and (d) ECG after stenting showed evidence of an anterior myocardial infarction.

Figure 2.

Coronary angiography of a male patient in his early 60s who presented with intermittent compression chest pain for 3 days, as well as radiating pain in his shoulders and back: (a) coronary angiography prior to stenting showed severe coronary artery disease affecting the proximal left anterior descending artery (LAD) and (b) post-stenting coronary angiography with LAD detail.

This study complied with the Declaration of Helsinki. All patient details were de-identified. The patient provided written consent to treatment. The reporting of this study conforms to CARE guidelines. ⁴

Discussion

It is critical to diagnose Wellens’ syndrome early. Its ECG characteristics can be categorized into two types: type B, which displays symmetrical and deeply inverted T waves in precordial chest leads (75% of patients); and type A, which is characterized by biphasic T waves in V2–V3 (25% of cases). ⁵ These ECG abnormalities may revert to normal or result in ST segment elevation, or even shift from type A to type B, ³ which may occur during the painless period or chest discomfort. The cause of the ECG alterations is not fully understood. Some theories suggest that the spontaneous reperfusion of the LAD may lead to the process of myocardial stunning due to the acute obstruction of atherosclerotic plaque, coronary artery spasm or microvascular disease.^3,6 A previous study has suggested that T-wave changes in patients with Wellens’ syndrome are associated with increased myocardial mechanical and electrical dispersion. ⁷ The ECG alterations could be transient, last a few months or they might disappear once the treatment is over. ⁸ T-wave inversion is not the same as Wellens’ syndrome on its own. Precordial T-wave inversion can have many distinct causes, such as Takotsubo cardiomyopathy, persistent thromboembolic pulmonary hypertension, cocaine-induced coronary vasospasm, cerebral haemorrhage, left ventricular hypertrophy and pulmonary embolism. ⁹ This current case is rare because it records the detailed evolution of a patient's ECG from Wellens’ syndrome to acute anterior myocardial infarction. A similar case has been reported previously. ¹⁰ Although the patient underwent urgent coronary angiography and stenting, his cardiac function was affected. If Wellens’ syndrome can be identified earlier, patients might have a better prognosis.

In conclusion, emergency physicians should promptly diagnose Wellens’ syndrome and perform revascularization as soon as possible. Early recognition and proactive intervention are crucial, as they may help to alleviate adverse consequences. ¹¹